1. A new method has been developed for measuring the total antioxidant capacity of body fluids and drug solutions, based on the absorbance of the ABTS*+ radical cation. 2. An automated method for use on a centrifugal analyser, as well as a manual method, is described. 3. The procedure has been applied to physiological antioxidant compounds and radical-scavenging drugs, and an antioxidant ranking was established based on their reactivity relative to a 1.0 mmol/l Trolox standard. 4. The Trolox equivalent antioxidant capacity of plasma from an adult reference population has been measured, and the method optimized and validated. 5. The method has been applied to investigate the total plasma antioxidant capacity of neonates and how this may be compromised in prematurity.

To study the cellular infiltrate that occurs within the airways of infants with respiratory syncytial virus bronchiolitis, samples of airways secretions were obtained by bronchial lavage from the lower respiratory tract of infants ventilated for this condition and from the upper airway of non-intubated infants with this disorder using nasopharyngeal aspirates.Cytospin samples were prepared so that differential cell counts could be performed on the cells obtained and alkaline phosphatase-antialkaline phosphatase immunocytochemical analysis of lymphocyte subsets was carried out using a panel of monoclonal antibodies, which included anti-CD3, anti-CD4, anti-CD8, anti-CD19, and anti-TcR-y.Results from the lower and upper airways were similar. Large numbers of inflammatory cells were obtained, of which neutrophils accounted for a median of 93%/o in the upper airway and 76% in the lower airway. The numbers of CD8 positive cells detected were small and consistently less than CD4 positive cells, median CD4:CD8 ratios being 22*5:1 and 15:1 for the lower and upper airways. CD19 positive cells were rarely observed and no y8 positive lymphocytes were detected.These results indicate that neutrophils probably play a major part in causing symptoms in these infants. They do not support the concept that excessive lymphocyte mediated cytotoxic activity is principally responsible for the pathology in respiratory syncytial virus bronchiolitis. (Arch Dis Child 1994; 71: 428-432) The respiratory syncytial virus is unique in its ability to cause yearly epidemics of respiratory disease.1 2 As a result almost all infants will have been infected by the virus by the second year of life and, of these, 05-2% develop acute bronchiolitis severe enough to be admitted to hospital. Results from studies using a formalin inactivated virus3 and other more recent attempts to produce a vaccine suggest that it is unlikely that we will be able to effectively prevent this distressing illness until the immunological mechanisms involved in the disease process, including those aspects conferring protection, are clarified.

In order to evaluate further the relationship between acute bronchiolitis in infancy and subsequent respiratory problems, children prospectively followed up from the time of their admission to hospital were reviewed along with a group of matched controls recruited at the previous five and a half year assessment. Sixty one index children and 47 controls took part. The groups were well matched for age, height, parental smoking, and social class. Although the prevalence of respiratory symptoms had fallen when related to the previous review, there remained an excess of coughing (48 and 17% in index and control children respectively; odds ratio 4.02) and wheezing (34 and 13% in index and control children respectively; odds ratio 3.59). Bronchodilator therapy was used by 33% of index children compared with 3% of controls. Lung function tests revealed no significant diVerences in the measurements of lung growth-for example, forced vital capacity, functional residual capacity, and total lung capacity-but the index children had significant reductions in measurements of airways obstruction-for example, forced expiratory volume in one second, maximum expiratory flow at 75, 50 and 25% of vital capacity, and airways resistance. Family history and personal skin tests showed no excess of atopy in the index group. This study supports the claim that the excess respiratory symptoms after acute bronchiolitis are not due to familial or personal susceptibility to atopy.

Extremely low birth weight premature infants have been known for many years to have limited antioxidant protective capacity, especially with reference to those antioxidant components which do not cross the placenta until the third trimester of gestation. In this study the total antioxidant activity and the concentrations of individual antioxidants in plasma from premature neonates (27 f 2 weeks gestation) compared to term babies (3841 weeks gestation) have been examined. The results show elevated levels of ascorbate at birth in the plasma of premature neonates compared with those of term babies, but the total plasma antioxidant status of the premature babies is significantly lower than that of term babies. At 5 days post-partum the ascorbate levels are within the normal adult range and plasma bilirubin levels are considerably enhanced in both groups, while the total plasma antioxidant status of the premature neonates has increased. Analysis of the relationship between the total plasma antioxidant activity and the bilirubin concentration show a direct, highly significant correlation for the term group, r* = 0.774, consistent with significance of bilirubin as a plasma antioxidant.

As part of a long term prospective study, 73 children who had been admitted to hospital with viral bronchiolitis as infants, were reviewed 5-5 years later and compared with a carefully matched control group. In the postbronchiolitis group, there was a highly significant increase in respiratory symptoms including wheezing (42.5% v 15-0%, relative risk=2-8).Although atopy in the family was not significantly increased in the index group, personal atopy was more prevalent. However, personal atopy was not significantly more prevalent in the symptomatic postbronchiolitis, compared with those who were symptom free, and so did not account for the high prevalence of postbronchiolitis wheezing in this cohort. In addition, in a stepwise logistic regressional model, bronchiolitis remained a significant predictor of wheezing after adjusting for potential confounding variables, including atopy. Bronchial responsiveness to histamine was significantly increased in the index group. However, no significant relationship of positive tests to wheezing could be demonstrated, and a high rate of positive responses was noted in the controls.